Abstract |
Bufalin is a natural toxin with anti-leukemic properties. It induces cell differentiation and apoptosis, as well as increasing the sensitivity of leukemia cells to other chemotherapeutic agents. We investigated the biological effects and molecular mechanisms of bufalin triggered apoptosis in HL-60 cells by gene expression profiling. The broad transcriptional response to bufalin was consistent with bufalin's action of regulating HL-60 cell proliferation and apoptosis, as well as its synergistic effect with other drugs. Further transcription factor ELISA experiments suggested that the transcription factors NFkappaB and AP-1 were activated to promote bufalin-induced HL-60 cell apoptosis. Our study provides new insights into the molecular mechanisms of bufalin, might prove to be beneficial in leukemia therapy.
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Authors | Ailiang Chen, Jian Yu, Liang Zhang, Yimin Sun, Yan Zhang, Hongyan Guo, Yuxiang Zhou, Keith Mitchelson, Jing Cheng |
Journal | Biotechnology letters
(Biotechnol Lett)
Vol. 31
Issue 4
Pg. 487-94
(Apr 2009)
ISSN: 1573-6776 [Electronic] Netherlands |
PMID | 19039527
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Chemical References |
- Bufanolides
- NF-kappa B
- Transcription Factor AP-1
- bufalin
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Topics |
- Apoptosis
- Bufanolides
(toxicity)
- Cell Proliferation
(drug effects)
- Gene Expression Profiling
- HL-60 Cells
- Humans
- NF-kappa B
(biosynthesis)
- Oligonucleotide Array Sequence Analysis
- Transcription Factor AP-1
(biosynthesis)
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